Advantages of NMNH
NMNH: 1. “Bonzyme” Whole-enzymatic method, environmental-friendly, no harmful solvent residues manufacturing powder. 2. Bontac is a very first manufacture in the world to produce the NMNH powder on the level of high purity, stability. 3. Exclusive “Bonpure” seven-step purification technology, high purity（up to 99%) and stability of production of NMNH powder 4. Self-owned factories and obtained a number of international certifications to ensure high quality and stable supply of products of NMNH powder 5. Provide one-stop product solution customization service
Advantages of NADH
NADH: 1. Bonzyme whole-enzymatic method, environmental-friendly, no harmful solvent residues 2. Exclusive Bonpure seven-step purification technology, purity up higher than 98 % 3. Special patented process crystal form, higher stability 4. Obtained a number of international certifications to ensure high quality 5. 8 domestic and foreign NADH patents, leading the industry 6. Provide one-stop product solution customization service
Advantages of NAD
NAD: 1. “Bonzyme” Whole-enzymatic method, environmental-friendly, no harmful solvent residues 2. Stable supplier of 1000+ enterprises around the world 3. Unique “Bonpure” seven-step purification technology, higher product content and higher conversion rate 4. Freeze drying technology to ensure stable product quality 5. Unique crystal technology, higher product solubility 6. Self-owned factories and obtained a number of international certifications to ensure high quality and stable supply of products
Advantages of MNM
NMN: 1. “Bonzyme”Whole-enzymatic method, environmental-friendly, no harmful solvent residues 2. Exclusive“Bonpure”seven-step purification technology, high purity（up to 99.9%) and stability 3. Industrial leading technology: 15 domestic and international NMN patents 4. Self-owned factories and obtained a number of international certifications to ensure high quality and stable supply of products 5. Multiple in vivo studies show that Bontac NMN is safe and effective 6. Provide one-stop product solution customization service 7. NMN raw material supplier of famous David Sinclair team of Harvard University
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Bontac Bio-Engineering (Shenzhen) Co., Ltd. (hereafter referred to as BONTAC) is a high-tech enterprise established in July 2012. BONTAC integrates R&D, production and sales, with enzyme catalysis technology as the core and coenzyme and natural products as main products. There are six major series of products in BONTAC, involving coenzymes, natural products, sugar substitutes, cosmetics, dietary supplements and medical intermediates.
As the leader of the global NMN industry, BONTAC has the first whole-enzyme catalysis technology in China. Our coenzyme products are widely used in health industry, medical & beauty, green agriculture, biomedicine and other fields. BONTAC adheres to independent innovation, with more than 170 invention patents. Different from the traditional chemical synthesis and fermentation industry, BONTAC has advantages of green low-carbon and high-value-added biosynthesis technology. What’s more, BONTAC has established the first coenzyme engineering technology research center at the provincial level in China which also is the sole in Guangdong Province.
In the future, BONTAC will focus on its advantages of green, low-carbon and high-value-added biosynthesis technology, and build ecological relationship with academia as well as upstream/downstream partners, continuously leading the synthetic biological industry and creating a better life for human beings.
BONTAC NMNH product features and advantages
1. "Bonzyme" Whole-enzymatic method, environmental-friendly, no harmful solvent residues manufacturing powder.
2. Bontac is a very first manufacture in the world to produce the NMNH powder on the level of high purity, stability.
3. Exclusive “Bonpure” seven-step purification technology, high purity (up to 99%) and stability of production of NMNH powder
4. Self-owned factories and obtained a number of international certifications to ensure high quality and stable supply of products of NMNH powder
5. Provide one-stop product solution customization service
NMNH is more potent than NMN
When applied to cultured cells, the NMNH is shown to be more efficient than NMN as it was able to “significantly increase NAD+ at a ten times lower concentration (5 µM) than that needed for NMN”. Moreover, NMNH shows to be more effective , as at 500 µM concentration, it achieved “an almost 10-fold increase in the NAD+ concentration, while NMN was only able to double NAD+ content in these cells, even at 1 mM concentration.”.
Interestingly, NMNH also appears to act quicker and has a longer-lasting effect compared to NMN. According to the authors, NMNH induces a “significant increase in NAD+ levels within 15 minutes”, and “NAD+ steadily increased for up to 6 hours and remained stable for 24 hours, while NMN reached its plateau after only 1 hour, most likely because the NMN recycling pathways to NAD+ had already become saturated.”.
NADH powder manufacturing method
The main methods of NMNH powder preparation include extraction, fermentation, fortification, biosynthesis and organic matter synthesis. Compared with other preparations, the whole enzyme becomes the mainstream method owing to the advantages of pollution free, high level of purity and
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Frequently Asked Question
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NADH is synthesized by the body and thus is not an essential nutrient. It does require the essential nutrient nicotinamide for its synthesis, and its role in energy production is certainly an essential one. In addition to its role in the mitochondrial electron transport chain, NADH is produced in the cytosol. The mitochondrial membrane is impermeable to NADH, and this permeability barrier effectively separates the cytoplasmic from the mitochondrial NADH pools. However, cytoplasmic NADH can be used for biologic energy production. This occurs when the malate-aspartate shuttle introduces reducing equivalents from NADH in the cytosol to the electron transport chain of the mitochondria. This shuttle mainly occurs in the liver and heart.
Nicotinamide adenine dinucleotide (NAD+ ) homeostasis is constantly compromised due to degradation by NAD+ -dependent enzymes. NAD+ replenishment by supplementation with the NAD+ precursors nicotinamide mononucleotide (NMN) and nicotinamide riboside (NR) can alleviate this imbalance. However, NMN and NR are limited by their mild effect on the cellular NAD+ pool and the need of high doses. Here, we report a synthesis method of a reduced form of NMN (NMNH), and identify this molecule as a new NAD+ precursor for the first time. We show that NMNH increases NAD+ levels to a much higher extent and faster than NMN or NR, and that it is metabolized through a different, NRK and NAMPT-independent, pathway. We also demonstrate that NMNH reduces damage and accelerates repair in renal tubular epithelial cells upon hypoxia/reoxygenation injury. Finally, we find that NMNH administration in mice causes a rapid and sustained NAD+ surge in whole blood, which is accompanied by increased NAD+ levels in liver, kidney, muscle, brain, brown adipose tissue, and heart, but not in white adipose tissue. Together, our data highlight NMNH as a new NAD+ precursor with therapeutic potential for acute kidney injury, confirm the existence of a novel pathway for the recycling of reduced NAD+ precursors and establish NMNH as a member of the new family of reduced NAD+ precursors.
First, inspect the factory. After some screening, NMNH companies that directly face consumers pay more attention to brand building. Therefore, for a good brand, quality is the most important thing, and the first thing to control the quality of raw materials is to inspect the factory. Bontac company actually manufacturing NMNH powder of high quality with the caterias of SGS. Secondly, the purity is tested. Purity is one of the most important parameters of NMN powder. If high purity NMNH cannot be guaranteed, the remaining substances are likely to exceed the relevant standards. As the attached certificates demonstrates that the NMNH powder produced by Bontac reach the purity of 99%. Finally, a professional test spectrum is needed to prove it. Common methods for determining the structure of an organic compound include Nuclear Magnetic Resonance Spectroscopy (NMR) and high-resolution mass spectrometry (HRMS). Usually through the analysis of these two spectra, the structure of the compound can be preliminarily determined.
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Unraveling Impacts of Ginsenoside Rg3 Treatment on IL-1β-induced Injury of NPCs
Introduction Intervertebral disc degeneration (IDD) is a frequently seen orthopedic disease, which is accompanied with excessive apoptosis of nucleus pulposus cells (NPCs) and degeneration of extracellular matrix (ECM), with main symptoms of pain and numbness in the waist, legs and feet, as well as inflammation on and around the surface of bone tissues. Strikingly, ginsenoside Rg3, the main active ingredient of ginseng, has been attested to exhibit anti-catabolic and anti-apoptotic effects in IL-1β-treated human NPCs and IDD rats by inactivating the p38 MAPK pathway. The risk factors for IDD IDD is generally associated with risk factors such as aging, excessive exercise, working environment, and genetics. As one ages, the amount of water in the body and in the intervertebral discs will be reduced accordingly. Intervertebral discs that lack moisture will lose their elastic function and become hard. Once there is any stimulation or pressure, the intervertebral disc may crack, leading to intervertebral disc injury. For instance, the mechanical trauma caused by excessive exercise and work may accelerate the fragility of disc and exacerbate IDD. Anti-catabolic and anti-apoptotic effects of ginsenoside Rg3 in IL-1β-treated human NPCs and IDD rats Ginsenoside Rg3 plays an anti-apoptotic role in IL-1β-treated human NPCs and IDD rats, as evidenced by the down-regulation of pro-apoptosis protein Bax and up-regulation of anti-apoptosis protein Bcl-2 in IL-1β-stimulated NPCs and IDD model rats. Besides, ginsenoside Rg3 represses ECM degradation in IL-1β-stimulated NPCs and intervertebral disc tissues of IDD rats, as attested by the decreased expression of ECM degradation-related factors MMPs (MMP2 and MMP3) and ADAMTSs (Adamts4, and Adamts5). Ginsenoside Rg3 exhibits anti-catabolic and anti-apoptotic effects in IL-1β-treated human NPCs. Ginsenoside Rg3 reduces apoptosis and catabolism in IDD rats. Alleviation of ginsenoside Rg3 in IDD via p38 MAPK pathway Ginsenoside Rg3 can alleviate NPC degeneration, recover the arrangement of annulus fibrous, and preserve more proteoglycan matrix via inactivating p38 MAPK pathway. In vitro, the fluorescence intensity of p38 is enhanced in IL-1β-stimulated NPCs, yet ginsenoside Rg3 offsets this promoting effect. In vivo, the phosphorylated p38 level is elevated in NPCs and the intervertebral disc tissues of IDD rats, while ginsenoside Rg3 works inversely. Ginsenoside Rg3 suppresses the IL-1β-stimulated p38 MAPK pathway in human NPCs Ginsenoside Rg3 inactivates the p38 MAPK pathway in IDD rats. Conclusion The anti-catabolic and anti-apoptotic effects of ginsenoside Rg3 in IL-1β treated human disc nucleus pulposus cells and in a rat model of disc degeneration are accomplished by inactivating the MAPK pathway, providing new clues on the treatment of IDD. Reference Chen J, Zhang B, Wu L, et al. Ginsenoside Rg3 exhibits anti-catabolic and anti-apoptotic effects in IL-1β treated human disc nucleus pulposus cells and in a rat model of disc degeneration by inactivating the MAPK pathway. Cell Mol Biol. 2024;70(1):233-238. doi:10.14715/cmb/2024.70.1.32 BONTAC Ginsenosides BONTAC has been dedicated to the R&D, manufacture and sale of raw materials for coenzyme and natural products since 2012, with self-owned factories, over 170 global patents as well as strong R&D team. BONTAC has rich R&D experience and advanced technology in the biosynthesis of rare ginsenosides Rh2/Rg3, with pure raw materials, higher conversion rate and higher content (up to 99%). One-stop service for customized product solution is available in BONTAC. With unique Bonzyme enzymatic synthesis technology, both S-type and R-type isomers can be accurately synthesized here, with stronger activity and precise targeting action. Our products are subjected to strict third-party self-inspection, which are worth of trustworthy. Disclaimer This article is based on the reference in the academic journal. The relevant information is provided for sharing and learning purposes only, and does not represent any medical advice purposes. If there is any infringement, please contact the author for deletion. The views expressed in this article do not represent the position of BONTAC. Under no circumstances will BONTAC be responsible or liable in any way for any claims, damages, losses, expenses or costs resulting or arising directly or indirectly from your reliance on the information and material on this website.
SLC25A51 Functions as an NAD+/NADH Redox Decoupler in AML
Introduction Solute carrier family 25 member 51 (SLC25A51) is perceived as a mammalian transporter, which is capable of importing oxidized nicotinamide adenine dinucleotide (NAD+) into mitochondrial matrix. Remarkably, upregulation of SLC25A51 has correlation with poorer outcomes in patients with acute myeloid leukemia (AML), a clinically aggressive haematological disease with a mortality rate of over 70% within the first 5 years following an initial diagnosis. The association between NAD+/NADH ratio and SLC25A51 in AML cells Both NAD+ (oxidative form) and NADH (reduced form) are essential coenzymes for cellular energy metabolism, and the ratio of NAD+/NADH reflects the metabolic activity and health state, which has a direct impact on cellular rhythms, senescence, carcinogenesis and death. Importing mitochondrial NAD+ by SLC25A51 could be a critical aspect supporting mitochondrial metabolism in AML tumorigenesis. Concretely, the decreased mitochondrial NAD+/NADH ratio and specific loss of reduced ubiquinol are observed post the depletion of SLC25A51 in AML cells U937. SLC25A51 as an NAD+/NADH redox decoupler in AML SLC25A51 functions as an NAD+/NADH redox decoupler in AML tumorigenesis to sustain an oxidative TCA cycle and promote glutaminolysis. Depletion of SLC25A51 results in increased usage of non-glutamine carbon sources to support the TCA cycle, as determined by increased proportions of unlabeled TCA intermediates. SLC25A51 is required for robust glutaminolysis. In the context of SLC25A51 depletion, AML cells are forced to rely more on glutamine for aspartate synthesis. Alleviation of AML by SLC25A51 depletion and 5-azacytidine Loss of SLC25A51 leads to a subcellular redistribution of NAD+ in AML cells to limit proliferation. The combination of SLC25A51 depletion and 5-azacytidine is much effective in repressing the viability of AML cells and prolonging the survival time of mice. Conclusion SLC25A51 can maintain mitochondrial oxidative phosphorylation and boost the proliferation of AML cells by regulating NAD+/NADH ratio in mitochondria, with promising efficacy in treating AML, especially in combination with 5-azacytidine. BONTAC NAD BONTAC has been dedicated to the R&D, manufacture and sale of raw materials for coenzyme and natural products since 2012, with self-owned factories, over 170 global patents as well as strong R&D team consisting of Doctors and Masters. BONTAC has rich R&D experience and advanced technology in the biosynthesis of NAD and its precursors (eg. NMN and NR), with various forms to be selected (eg. endoxin-free IVD-grade NAD, Na-free or Na-containing NAD; NR-CL or NR-Malate). High quality and stable supply of products can be better ensured here with the exclusive Bonpure seven-step purification technology and Bonzyme Whole-enzymatic method. Disclaimer This article is based on the reference in the academic journal. The relevant information is provided for sharing and learning purposes only, and does not represent any medical advice purposes. If there is any infringement, please contact the author for deletion. The views expressed in this article do not represent the position of BONTAC. Under no circumstances will BONTAC be held responsible or liable in any way for any claims, damages, losses, expenses, costs or liabilities whatsoever (including, without limitation, any direct or indirect damages for loss of profits, business interruption or loss of information) resulting or arising directly or indirectly from your reliance on the information and material on this website.
The Potential of Rg3-Loaded Hydrogel Scaffolds in Inhibiting Scar Formation Introduction
Introduction Ginsenoside Rg3 (Rg3) holds great promise as a potential drug for preventing scar formation, but it is often difficult for it to work alone due to its poor water solubility and low bioavailability. Herein, a novel Rg3-loaded dermal extracellular matrix (DECM) hydrogel scaffolds are prepared via 3D printing and nanoloading technologies, which improves the biosafety profile of Rg3 to a large extent, maintains a consistent local drug concentration for an extended duration and prolongs therapeutic effects, realizing the final goal of scar-free healing. The merits of 3D-printed DECM hydrogel scaffolds loaded with Rg3 3D-printed DECM hydrogel scaffolds have good supportability and stability. They could be folded into different shapes without obvious deformation or breakage, closely resembling the properties of natural skin. The continuous porous structure of DECM-2MSN scaffolds enables the faster transport of nutrients, oxygen, water, and metabolic wastes within the platform, which facilitates the wound healing. The uniqueness of 3D-printed DECM hydrogel scaffolds loaded with Rg3 Through decellularization, about 98.57% of dsDNA is removed from DECM, leaving few cellular remnants while preserving collagen in DECM, which simulates the natural extracellular matrix microenvironment for skin defect healing to the greatest extent, reducing the risk of immune rejection. Hydrogel exhibits excellent biocompatibility and solid-like rheological properties. Furthermore, mesoporous silica nanoparticles (MSNs) are introduced into the system to encase the Rg3 to control its release rate and enhance its bioavailability. The role of Rg3-loaded hydrogel scaffolds in wound healing The wound in DECM-2MSNs/Rg3 group has completely healed, exhibiting smooth and uniform regenerated epithelium with clear boundaries between the epidermis and dermis. During the wound healing process, Rg3 can suppress the excessive inflammation, hinder the formation of blood vessels, and prevent excessive and disordered proliferation of granulation tissue at the wound site, as manifested by the low expression of CD31, VEGF and TGF-β levels in DECM-2MSNs/Rg3 group. In the later stages of wound healing, Rg3 could repress collagen accumulation, thereby impeding scarring, without affecting the normal healing of the wound. Conclusion Rg3-loaded hydrogel scaffold can inhibit wound inflammation and collagen accumulation to repress scar formation. By integrating 3D bioprinting and nanoloading technologies to prepare this innovative wound dressing, the efficacy of Rg3 has been greatly improved, providing a novel therapeutic approach for scar-free wound healing. Reference Wang X, Wei P, Hu C, Zeng H, Fan Z. 3D printing of Rg3-loaded hydrogel scaffolds: anti-inflammatory and scar-formation related collagen inhibitory effects for scar-free wound healing. J Mater Chem B. Published online April 22, 2024. doi:10.1039/d3tb02941g BONTAC Ginsenosides BONTAC has been dedicated to the R&D, manufacture and sale of raw materials for coenzyme and natural products since 2012, with self-owned factories, over 170 global patents as well as strong R&D team. BONTAC has rich R&D experience and advanced technology in the biosynthesis of rare ginsenosides Rh2/Rg3, with pure raw materials, higher conversion rate and higher content (up to 99%). One-stop service for customized product solution is available in BONTAC. With unique Bonzyme enzymatic synthesis technology, both S-type and R-type isomers can be accurately synthesized here, with stronger activity and precise targeting action. Our products are subjected to strict third-party self-inspection, which are worth of trustworthy. Disclaimer This article is based on the reference in the academic journal. The relevant information is provided for sharing and learning purposes only, and does not represent any medical advice purposes. If there is any infringement, please contact the author for deletion. The views expressed in this article do not represent the position of BONTAC. Under no circumstances will BONTAC be held responsible or liable in any way for any claims, damages, losses, expenses, costs or liabilities whatsoever (including, without limitation, any direct or indirect damages for loss of profits, business interruption or loss of information) resulting or arising directly or indirectly from your reliance on the information and material on this website.